Motivated by the findings of some studies showing that T2D patients, in contrast to their improper glucagon response to oral glucose, are able to suppress glucagon release after an isoglycemic intravenous glucose infusion (IIGI) similarly to non-diabetic subjects, Lund et al. evaluated the role of GIP, GLP-1 and glucagon-like peptide-2 (GLP-2) in this discrepant response. Here, GIP is linked to type 2 diabetes mellitus.